Introduction
In December 2019, an outbreak of a coronavirus disease 2019 (COVID-19)
caused by the severe acute respiratory syndrome coronavirus 2
(SARS-CoV-2) first emerged in Wuhan, China [1,2]. The World Health
Organization declared a global pandemic on March 12, 2020, [3].
Since the first case was reported, COVID-19 has led to a significant
increase in morbidity and mortality worldwide. The researchers are
conducting several pharmacological studies against COVID-19 [4].
Among these research drugs, hydroxychloroquine (HQ), an antimalarial and
anti-rheumatic drug, received wide attention at first. However,
recently, its usage has remained in the background due to its side
effect profile. We included the HQ in the study to prove that
favipiravir’s arrhythmogenic effects were not inferior to HQ. Gautret et
al. showed a significant reduction of the nasopharyngeal viral carriage
in patients taking HQ [5]. Also, HQ inhibited SARS-CoV-2 activity in
vitro [6]. The point to be considered is the relationship between QT
prolongation with HQ [7]. Excessive prolongation of the QT interval
may trigger Torsade de Pointes (TdP). TdP is a form of polymorphic
ventricular tachycardia that can transform into ventricular fibrillation
[8]. Furthermore, HQ directly contributes to myocardial suppression
[9].
Favipiravir is a currently available drug being researched for COVID-19
treatment [10]. Essentially, favipiravir was approved for
drug-resistant influenza treatment in 2014 in Japan [11]. It blocks
viral replication by inhibiting the viral RNA-dependent RNA polymerase
[12]. Therefore, favipiravir may also exert antiviral activity on
SARS-CoV-2, an RNA virus. Recent studies have redesigned favipiravir to
use in COVİD-19 treatment. In a recent in vitro study, Wang and
colleagues found that favipiravir reduced viral replication [13]. A
recent study demonstrated that favipiravir was associated with a shorter
time to viral clearance and a higher recovery rate on chest scanning
[14]. Chen et al. reported that favipiravir had a faster recovery
period than umifenovir in COVID-19 patients [15]. Studies have
reported that favipiravir is well tolerated and has a good safety
profile [16,17]. Diarrhea, hyperuricemia, and elevated liver enzymes
were the most frequent adverse effects reported in clinical trials
[14,18]. Besides, Ghasemiyeh et al. revealed that favipiravir was
infrequently associated with drug-induced psychotic symptoms [16].
Contrary to studies reporting that favipiravir has a well-established
safety profile, we observed frequent conduction disorders in our
patients. This study investigates the arrhythmogenic adverse effects of
favipiravir in COVID-19 patients by comparing it with HQ, the best-known
culprit in this regard.